001     282288
005     20251114124359.0
024 7 _ |a 10.1177/13872877251379466
|2 doi
024 7 _ |a pmid:41004660
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024 7 _ |a 1387-2877
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024 7 _ |a 1875-8908
|2 ISSN
037 _ _ |a DZNE-2025-01259
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Tanaka, Emi
|b 0
245 _ _ |a Modulation of middle-latency somatosensory evoked magnetic field waveforms associated with the pathophysiological states of Alzheimer's disease.
260 _ _ |a Amsterdam
|c 2025
|b IOS Press
336 7 _ |a article
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336 7 _ |a Journal Article
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a BackgroundAlzheimer's disease (AD) frequently causes epilepsy and myoclonus. These symptoms are thought to be associated with neuronal hyperexcitability, highlighting the need for biomarkers that reflect synaptic functional alterations.ObjectiveWe aimed to examine changes in neuronal excitability associated with AD progression using magnetoencephalography (MEG). Furthermore, we investigated the relationship between alterations in electromagnetic signals and other neuroimaging biomarkers.MethodsWe measured middle-latency somatosensory evoked magnetic fields (m-SEFs) following right median nerve stimulation in 45 individuals, comprising 6, 8, and 31 individuals with AD dementia (ADD), mild cognitive impairment (MCI), and cognitively healthy older adults, respectively. Cortical reactivity relative to the primary somatosensory response (N20 m) was assessed using normalized m-SEF waveforms. Additionally, we analyzed associations between these waveforms and amyloid-β (Aβ) deposition, regional glucose metabolism, and gray matter volume using positron-emission tomography and magnetic resonance imaging.ResultsThe m-SEF waveform exhibited six components (M2-M7) within 150 ms of the N20 m (M1) response. The m-SEF waveforms tended to be enlarged in ADD and MCI, with a significant enhancement of M2 in ADD. The amplitude of M7 at approximately 100 ms latency was significantly and positively correlated with local Aβ deposition in the sensorimotor cortex. Moreover, regional glucose hypometabolism in the hippocampus and pulvinar was significantly associated with enlargement of the M4, M6, and M7 components.ConclusionsThese findings indicate that cortical responses to somatosensory stimulation are modulated by AD progression. M-SEF may serve as a potential marker for evaluating cortical excitability in the sensorimotor cortex.
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650 _ 7 |a Alzheimer's disease
|2 Other
650 _ 7 |a amyloid-β protein
|2 Other
650 _ 7 |a cortical excitability
|2 Other
650 _ 7 |a evoked potentials
|2 Other
650 _ 7 |a glucose metabolism
|2 Other
650 _ 7 |a magnetoencephalography
|2 Other
650 _ 7 |a somatosensory
|2 Other
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Alzheimer Disease: physiopathology
|2 MeSH
650 _ 2 |a Alzheimer Disease: diagnostic imaging
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Evoked Potentials, Somatosensory: physiology
|2 MeSH
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Magnetoencephalography
|2 MeSH
650 _ 2 |a Magnetic Resonance Imaging
|2 MeSH
650 _ 2 |a Positron-Emission Tomography
|2 MeSH
650 _ 2 |a Aged, 80 and over
|2 MeSH
650 _ 2 |a Cognitive Dysfunction: physiopathology
|2 MeSH
650 _ 2 |a Cognitive Dysfunction: diagnostic imaging
|2 MeSH
650 _ 2 |a Median Nerve: physiopathology
|2 MeSH
650 _ 2 |a Middle Aged
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Somatosensory Cortex: physiopathology
|2 MeSH
700 1 _ |a Nihashi, Takashi
|b 1
700 1 _ |a Kato, Takashi
|b 2
700 1 _ |a Arahata, Yutaka
|0 0000-0001-7810-8984
|b 3
700 1 _ |a Takeda, Akinori
|b 4
700 1 _ |a Sakurai, Keita
|b 5
700 1 _ |a Yokoi, Katsunori
|b 6
700 1 _ |a Iwata, Kaori
|b 7
700 1 _ |a Diers, Kersten
|0 P:(DE-2719)2812059
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700 1 _ |a Maess, Burkhard
|b 9
700 1 _ |a Nakamura, Akinori
|0 0000-0002-4259-1297
|b 10
773 _ _ |a 10.1177/13872877251379466
|g Vol. 108, no. 2, p. 862 - 872
|0 PERI:(DE-600)2070772-1
|n 2
|p 862 - 872
|t Journal of Alzheimer's disease
|v 108
|y 2025
|x 1387-2877
856 4 _ |u https://pub.dzne.de/record/282288/files/DZNE-2025-01259_Restricted.pdf
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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